Glial swelling with eosinophilia in human post-mortem brains : a change indicative of plasma extravasation

• Published in: Acta neuropathologica Vol. 100; no. 6; pp. 688 - 694
• Main Authors: DEL BIGIO, M. R, DECK, J. H. N, DAVIDSON, G. S
• Format: Journal Article
• Language: English
• Published: Berlin Springer 01-12-2000; Springer Nature B.V
• Subjects: Adolescent; Adult; Aged; Animals; Astrocytes; Autopsy; Biological and medical sciences; Blood diseases; Brain - metabolism; Brain - pathology; Brain - physiopathology; Brain Edema - etiology; Brain Edema - pathology; Brain Edema - physiopathology; Capillary Permeability - physiology; Cell Death - physiology; Edema; Eosinophilia; Eosinophilia - etiology; Eosinophilia - pathology; Eosinophilia - physiopathology; Extravasation; Fibrinogen; Glia; Glial cells; Glial fibrillary acidic protein; Hemorrhage; Humans; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Intracranial Hemorrhages - complications; Intracranial Hemorrhages - pathology; Intracranial Hemorrhages - physiopathology; Leukocytes (eosinophilic); Macrophages; Medical sciences; Microglial cells; Middle Aged; Neuroglia - metabolism; Neuroglia - pathology; Neuroglia - ultrastructure; Neurology; Oligodendrocytes; Parenchyma; Perfusion; Plasma - metabolism; Plasma proteins; Postmortem Changes; Rats; Substantia alba; Vascular diseases and vascular malformations of the nervous system; Human; Immunohistochemistry; Nervous system diseases; Rat; Neuroglia; Rodentia; Postmortem; Cardiovascular disease; Exploration; Eosinophilia; Cerebral disorder; Vascular disease; Pathology; Vertebrata; Mammalia; Animal; Cerebral hemorrhage; Central nervous system disease; Cerebral edema; Cerebrovascular disease
• ISSN: 0001-6322; 1432-0533
• DOI: 10.1007/s004010000236

Swollen, intensely eosinophilic glial cells are often observed in the vicinity of hemorrhagic lesions in post-mortem human brains. We sought to determine the nature of this change. Thirty adult human brains removed at autopsy and three surgical specimens were obtained 6h to 60 days following a hemorrhagic event. They were subjected to a battery of histochemical and immunohistochemical stains. The swollen cells, which were observed in the majority of autopsy specimens in which hemorrhage had occurred within the previous 9 days, stained intensely red with Masson stain and were immunoreactive for IgG, IgM, IgA, and fibrinogen. Some were also immunoreactive for glial fibrillary acidic protein, particularly in subpial and subependymal areas, if the lesions were more than 3 days old. In white matter some of the cells were immunoreactive for CNPase. There was no labeling with markers for macrophage/microglial cells. The absence of DNA fragment detection by TUNEL suggests that the cells were not dying. Mild glial cytoplasmic eosinophilia without swelling was observed in surgical specimens. No eosinophilic swollen glia were seen in perfusion-fixed rat brains with experimental intracerebral hemorrhage, although they were seen in rat brains that were not promptly fixed. We conclude that human macroglia, including astrocytes and oligodendrocytes, ingest plasma proteins that have been released into brain parenchyma. This likely represents a homeostatic mechanism that maintains the composition of the extracellular environment. If the tissue is not promptly fixed the cells become more swollen and eosinophilic.